The strongly carcinogenic polycyclic hydrocarbons appear to be metabolically activated through the formation of vicinal diol-epoxides that are of the 'bay-region' type but recent evidence suggests that this precise mechanism may not necessarily apply in the case of weak or inactive compounds. We therefore propose to try to answer the following questions: Are vicinal diol-epoxides always involved in the metabolic activation of the polycyclic hydrocarbons, regardless of their carcinogenic potency? If so, are the diol-epoxides always of the 'bay-region' type? If not, what other species are involved? Can differences in the type of reactive intermediates formed account for differences in potency? Alternatively, can differences in the sites of attack and in the nature of the nucleic acid adducts formed in treated target tissues account for differences in activity within the polycyclic hydrocarbons as a class of chemical carcinogens? The answers will be sought using appropriate tissues and animal species together with cells and tissues maintained in culture and comparisons will be drawn between strongly and weakly active hydrocarbons using the battery of biochemical, biophysical and biological techniques that have contributed to recent progress in this area.